We examined the hypothesis that senescence represents a proximate mechanism by which the kidney is damaged in type 2 diabetic nephropathy (DN). As a first step, we studied whether the Senescence-Associated -Galactosidase (SA--Gal) and the cell cycle inhibitor p16^INK4A are induced in renal biopsies from patients with type 2 DN. SA--Gal staining was ~3 fold higher (p<0.05) than in controls (C) in the tubular compartment of diabetic kidneys and correlated directly with BMI and blood glucose. P16^INK4A expression was significantly increased in tubules (p<0.005) and in podocytes (P= 0.04). Nuclear P16^INK4A in glomeruli was associated with proteinuria (p < 0.002) while tubular p16^INK4A was directly associated with BMI, LDL-cholesterol and HbA₁C ( p<0.001-0.05). In a parallel set of experiments proximal tubule cells (PTEC) passaged under high glucose (HG) presented a limited life span and a ~2-fold increase in SA--Gal and p16^INK4A protein. Mean telomere (TRF) lengths decreased ~20% as an effect of replicative senescence. In addition, mean TRF decreased further by ~30% in cells cultivated under HG . Our results show that the kidney with type 2 DN displays an accelerated senescent phenotype in defined renal cell types, mainly tubule cells, and, to a less extent, podocytes and endothelia. A similar senescent pattern is observed when incubating PTECs under high glucose media. These changes are associated with shortening tubular telomere length in vitro. These findings indicate that diabetes may boost common pathways involving kidney cell senescence, thus reinforcing the role of the metabolic syndrome on biological ageing of tissues.